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朊病毒蛋白对于潜在学习和长期记忆保持是必需的。

Prion protein is necessary for latent learning and long-term memory retention.

作者信息

Nishida N, Katamine S, Shigematsu K, Nakatani A, Sakamoto N, Hasegawa S, Nakaoke R, Atarashi R, Kataoka Y, Miyamoto T

机构信息

Department of Bacteriology, Nagasaki University School of Medicine, Japan.

出版信息

Cell Mol Neurobiol. 1997 Oct;17(5):537-45. doi: 10.1023/a:1026315006619.

DOI:10.1023/a:1026315006619
PMID:9353594
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11560205/
Abstract
  1. The cellular prion protein, designated PrPc, is a key molecule in the prion diseases but its physiological function remains unknown. To elucidate whether PrPc plays some role in the central nervous system, we established a line of mice in which the PrP gene had been disrupted and subsequently conducted long-term observations. 2. Performance in latent learning and passive avoidance was evaluated using water-finding and step-through tests, respectively. 3. PrP-/- mice showed impaired performance in the water-finding test, indicating a disturbance in latent learning, at 23 weeks of age. In the step-through test, although the PrP-/- mice showed normal learning ability and short-term memory retention, they evidenced a significant disturbance in long-term memory retention. 4. These results indicate that PrPc is needed for certain types of learning and memory and that the loss of function of this protein may contribute to the pathogenesis of prion diseases.
摘要
  1. 细胞朊蛋白,称为PrPc,是朊病毒疾病中的关键分子,但其生理功能仍不清楚。为了阐明PrPc是否在中枢神经系统中发挥某种作用,我们建立了一个PrP基因已被破坏的小鼠品系,并随后进行了长期观察。2. 分别使用找水试验和穿梭试验评估潜在学习和被动回避的表现。3. PrP-/-小鼠在23周龄时在找水试验中表现受损,表明潜在学习受到干扰。在穿梭试验中,虽然PrP-/-小鼠表现出正常的学习能力和短期记忆保持,但它们在长期记忆保持方面明显受到干扰。4. 这些结果表明,PrPc是某些类型的学习和记忆所必需的,并且这种蛋白质的功能丧失可能导致朊病毒疾病的发病机制。

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1
Prion protein is necessary for latent learning and long-term memory retention.朊病毒蛋白对于潜在学习和长期记忆保持是必需的。
Cell Mol Neurobiol. 1997 Oct;17(5):537-45. doi: 10.1023/a:1026315006619.
2
Impaired motor coordination in mice lacking prion protein.缺乏朊病毒蛋白的小鼠运动协调性受损。
Cell Mol Neurobiol. 1998 Dec;18(6):731-42. doi: 10.1023/a:1020698305911.
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Cellular prion protein ablation impairs behavior as a function of age.
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Analysis of co-isogenic prion protein deficient mice reveals behavioral deficits, learning impairment, and enhanced hippocampal excitability.分析同基因朊病毒蛋白缺失小鼠揭示了行为缺陷、学习障碍和增强的海马兴奋性。
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Prion protein is necessary for normal synaptic function.朊病毒蛋白对于正常的突触功能是必需的。
Nature. 1994 Jul 28;370(6487):295-7. doi: 10.1038/370295a0.
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Novel mechanisms of degeneration of the central nervous system--prion structure and biology.中枢神经系统变性的新机制——朊病毒结构与生物学
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7
Immunization with either prion protein fragment 95-123 or the fragment-specific antibodies rescue memory loss and neurodegenerative phenotype of neurons in olfactory bulbectomized mice.用朊病毒蛋白片段 95-123 或片段特异性抗体进行免疫接种可挽救嗅球切除术小鼠神经元的记忆丧失和神经退行性表型。
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On the biology of prions.论朊病毒生物学
Acta Neuropathol. 1987;72(4):299-314. doi: 10.1007/BF00687261.
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Ectopic expression of prion protein (PrP) in T lymphocytes or hepatocytes of PrP knockout mice is insufficient to sustain prion replication.在朊病毒蛋白(PrP)基因敲除小鼠的T淋巴细胞或肝细胞中异位表达朊病毒蛋白不足以维持朊病毒复制。
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Post-natal knockout of prion protein alters hippocampal CA1 properties, but does not result in neurodegeneration.朊病毒蛋白的产后敲除会改变海马CA1区的特性,但不会导致神经退行性变。
EMBO J. 2002 Feb 1;21(3):202-10. doi: 10.1093/emboj/21.3.202.

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Cureus. 2024 Nov 5;16(11):e73063. doi: 10.7759/cureus.73063. eCollection 2024 Nov.
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N-Terminal Regions of Prion Protein: Functions and Roles in Prion Diseases.朊病毒蛋白的 N 端结构域:在朊病毒病中的功能和作用。
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An ancient conserved role for prion protein in learning and memory.朊病毒蛋白在学习和记忆中的古老保守作用。
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What Is Our Current Understanding of PrP-Associated Neurotoxicity and Its Molecular Underpinnings?我们目前对与朊蛋白(PrP)相关的神经毒性及其分子基础有哪些了解?
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The biological function of the cellular prion protein: an update.细胞朊蛋白的生物学功能:最新进展
BMC Biol. 2017 May 2;15(1):34. doi: 10.1186/s12915-017-0375-5.
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Behavioral abnormalities in prion protein knockout mice and the potential relevance of PrP(C) for the cytoskeleton.朊病毒蛋白基因敲除小鼠的行为异常以及细胞朊蛋白(PrP(C))与细胞骨架的潜在相关性
Prion. 2014;8(6):381-6. doi: 10.4161/19336896.2014.983746.
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本文引用的文献

1
Control of memory formation through regulated expression of a CaMKII transgene.通过钙调蛋白激酶II转基因的调控表达来控制记忆形成。
Science. 1996 Dec 6;274(5293):1678-83. doi: 10.1126/science.274.5293.1678.
2
Hippocampal slices from prion protein null mice: disrupted Ca(2+)-activated K+ currents.来自朊病毒蛋白缺失小鼠的海马切片:钙激活钾电流紊乱。
Neurosci Lett. 1996 May 3;209(1):49-52. doi: 10.1016/0304-3940(96)12596-9.
3
Loss of cerebellar Purkinje cells in aged mice homozygous for a disrupted PrP gene.
Nature. 1996 Apr 11;380(6574):528-31. doi: 10.1038/380528a0.
4
Altered circadian activity rhythms and sleep in mice devoid of prion protein.缺乏朊病毒蛋白的小鼠的昼夜活动节律和睡眠发生改变。
Nature. 1996 Apr 18;380(6575):639-42. doi: 10.1038/380639a0.
5
Age-related deterioration in conditional avoidance task in the SAM-P/10 mouse, an animal model of spontaneous brain atrophy.SAM-P/10小鼠是自发性脑萎缩的动物模型,其在条件性回避任务中存在与年龄相关的功能衰退。
Brain Res. 1993 Apr 16;608(2):266-72. doi: 10.1016/0006-8993(93)91467-7.
6
Prion protein is strongly immunolocalized at the postsynaptic domain of human normal neuromuscular junctions.朊病毒蛋白在人类正常神经肌肉接头的突触后区域有强烈的免疫定位。
Neurosci Lett. 1993 Sep 3;159(1-2):111-4. doi: 10.1016/0304-3940(93)90811-x.
7
Correlations between immediate early gene induction and the persistence of long-term potentiation.
Neuroscience. 1993 Oct;56(3):717-27. doi: 10.1016/0306-4522(93)90369-q.
8
Prion diseases and neurodegeneration.朊病毒病与神经退行性变。
Annu Rev Neurosci. 1994;17:311-39. doi: 10.1146/annurev.ne.17.030194.001523.
9
Prion protein is necessary for normal synaptic function.朊病毒蛋白对于正常的突触功能是必需的。
Nature. 1994 Jul 28;370(6487):295-7. doi: 10.1038/370295a0.
10
129/Ola mice carrying a null mutation in PrP that abolishes mRNA production are developmentally normal.携带PrP基因无效突变(该突变消除mRNA产生)的129/Ola小鼠发育正常。
Mol Neurobiol. 1994 Apr-Jun;8(2-3):121-7. doi: 10.1007/BF02780662.